Effects of cpxR on the growth characteristics and antibiotic production of Xenorhabdus nematophila

Abstract

Summary CpxR is a global response regulator that negatively influences the antimicrobial activities of Xenorhabdus nematophila . Herein, the wildtype and Δ cpxR mutant of X. nematophila were cultured in a 5‐l and 70‐l bioreactor. The kinetic analysis showed that Δ cpxR significantly increased the cell biomass and antibiotic activity. The maximum dry cell weight ( DCW ) and antibiotic activity of Δ cpxR were 20.77 ± 1.56 g L −1 and 492.0 ± 31.2 U ml −1 and increased by 17.28 and 97.33% compared to the wildtype respectively. Xenocoumacin 1 (Xcn1), a major antimicrobial compound, was increased 3.07‐fold, but nematophin was decreased by 48.7%. In 70‐l bioreactor, DCW was increased by 18.97%, while antibiotic activity and Xcn1 were decreased by 27.71% and 11.0% compared to that in 5‐l bioreactor respectively. Notably, pH had remarkable effects on the cell biomass and antibiotic activity of Δ cpxR , where Δ cpxR was sensitive to alkaline pH conditions. The optimal cell growth and antibiotic activity of Δ cpxR occurred at pH 7.0, while Xcn1 was increased 5.45‐ and 3.87‐fold relative to that at pH 5.5 and 8.5 respectively. These findings confirmed that Δ cpxR considerably increased the biomass of X. nematophila at a late stage of fermentation. In addition, Δ cpxR significantly promoted the biosynthesis of Xcns but decreased the production of nematophin.

Increasing the Production of Xenocoumacin 1 by Optimizing the Fermentation Process of Xenorhabdus Nematophila

“…In addition, transcription regulator OmpR negatively regulates xcnA-L genes expression while positively regulates xcnMN expression, which led to a 3.3 fold yield of Xcn1 in ΔompR mutant [25]. Interestingly, transcription regulator CpxR not only regulates the biosynthesis of Xcn1 with the same regulation model of OmpR, but also positively regulates ompR transcription [28,29]. Nonetheless, it is unclear that how transcription regulator OmpR and CpxR regulate Xcn1 biosynthesis in molecular level.…”